Longitudinal Retinal Changes in MOGAD

with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group

doi:10.1002/ana.26440

Longitudinal Retinal Changes in MOGAD

with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group

Charité – Universitätsmedizin Berlin
University of California at San Francisco
Johns Hopkins University
University of Utah
K.S. Hegde Medical Academy
Université de Lille
Mayo Clinic Rochester, MN
Medical University of Vienna
Ludwig Maximilian University of Munich
Heinrich Heine University Düsseldorf
Ruhr University Bochum
Sechenov First Moscow State Medical University
Technical University of Munich
Lillebaelt & Slagelse Hospitals
University of Southern Denmark
Hôpital neurologique et neurochirurgical Pierre Wertheimer
Hospital Universitari Vall d'Hebron
Hospital Clínic of Barcelona
University of California at Los Angeles
University of Michigan, Ann Arbor
University of California at Irvine

Research output: Contribution to journal › Article › peer-review

47 Scopus citations

Abstract

Objective: Patients with myelin oligodendrocyte glycoprotein antibody (MOG-IgG)-associated disease (MOGAD) suffer from severe optic neuritis (ON) leading to retinal neuro-axonal loss, which can be quantified by optical coherence tomography (OCT). We assessed whether ON-independent retinal atrophy can be detected in MOGAD. Methods: Eighty patients with MOGAD and 139 healthy controls (HCs) were included. OCT data was acquired with (1) Spectralis spectral domain OCT (MOGAD: N = 66 and HCs: N = 103) and (2) Cirrus high-definition OCT (MOGAD: N = 14 and HCs: N = 36). Macular combined ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) were quantified. Results: At baseline, GCIPL and pRNFL were lower in MOGAD eyes with a history of ON (MOGAD-ON) compared with MOGAD eyes without a history of ON (MOGAD-NON) and HCs (p < 0.001). MOGAD-NON eyes had lower GCIPL volume compared to HCs (p < 0.001) in the Spectralis, but not in the Cirrus cohort. Longitudinally (follow-up up to 3 years), MOGAD-ON with ON within the last 6–12 months before baseline exhibited greater pRNFL thinning than MOGAD-ON with an ON greater than 12 months ago (p < 0.001). The overall MOGAD cohort did not exhibit faster GCIPL thinning compared with the HC cohort. Interpretation: Our study suggests the absence of attack-independent retinal damage in patients with MOGAD. Yet, ongoing neuroaxonal damage or edema resolution seems to occur for up to 12 months after ON, which is longer than what has been reported with other ON forms. These findings support that the pathomechanisms underlying optic nerve involvement and the evolution of OCT retinal changes after ON is distinct in patients with MOGAD. ANN NEUROL 2022;92:476–485.

Original language	English
Pages (from-to)	476-485
Number of pages	10
Journal	Annals of Neurology
Volume	92
Issue number	3
DOIs	https://doi.org/10.1002/ana.26440
State	Published - Sep 2022

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10.1002/ana.26440

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@article{069afae567264c4598b9ea5b4cbe3e60,

title = "Longitudinal Retinal Changes in MOGAD",

abstract = "Objective: Patients with myelin oligodendrocyte glycoprotein antibody (MOG-IgG)-associated disease (MOGAD) suffer from severe optic neuritis (ON) leading to retinal neuro-axonal loss, which can be quantified by optical coherence tomography (OCT). We assessed whether ON-independent retinal atrophy can be detected in MOGAD. Methods: Eighty patients with MOGAD and 139 healthy controls (HCs) were included. OCT data was acquired with (1) Spectralis spectral domain OCT (MOGAD: N = 66 and HCs: N = 103) and (2) Cirrus high-definition OCT (MOGAD: N = 14 and HCs: N = 36). Macular combined ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) were quantified. Results: At baseline, GCIPL and pRNFL were lower in MOGAD eyes with a history of ON (MOGAD-ON) compared with MOGAD eyes without a history of ON (MOGAD-NON) and HCs (p < 0.001). MOGAD-NON eyes had lower GCIPL volume compared to HCs (p < 0.001) in the Spectralis, but not in the Cirrus cohort. Longitudinally (follow-up up to 3 years), MOGAD-ON with ON within the last 6–12 months before baseline exhibited greater pRNFL thinning than MOGAD-ON with an ON greater than 12 months ago (p < 0.001). The overall MOGAD cohort did not exhibit faster GCIPL thinning compared with the HC cohort. Interpretation: Our study suggests the absence of attack-independent retinal damage in patients with MOGAD. Yet, ongoing neuroaxonal damage or edema resolution seems to occur for up to 12 months after ON, which is longer than what has been reported with other ON forms. These findings support that the pathomechanisms underlying optic nerve involvement and the evolution of OCT retinal changes after ON is distinct in patients with MOGAD. ANN NEUROL 2022;92:476–485.",

author = "\{with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group\} and Oertel, \{Frederike Cosima\} and Sotirchos, \{Elias S.\} and Zimmermann, \{Hanna G.\} and Seyedamirhosein Motamedi and Svenja Specovius and Asseyer, \{Eva Susanna\} and Claudia Chien and Lawrence Cook and Eleni Vasileiou and Angeliki Filippatou and Calabresi, \{Peter A.\} and Shiv Saidha and Lekha Pandit and Anitha D'Cunha and Olivier Outteryck and H{\'e}l{\`e}ne Z{\'e}phir and Sean Pittock and Flanagan, \{Eoin P.\} and Bhatti, \{M. Tariq\} and Rommer, \{Paulus S.\} and Gabriel Bsteh and Tobias Zrzavy and Tania Kuempfel and Orhan Aktas and Marius Ringelstein and Philipp Albrecht and Ilya Ayzenberg and Thivya Pakeerathan and Benjamin Knier and Lilian Aly and Nasrin Asgari and Kerstin Soelberg and Romain Marignier and Tilikete, \{Caroline Froment\} and \{Cobo Calvo\}, Alvaro and Pablo Villoslada and Bernardo Sanchez-Dalmau and Martinez-Lapiscina, \{Elena H.\} and Sara Llufriu and Green, \{Ari J.\} and Yeaman, \{Michael R.\} and Smith, \{Terry J.\} and Brandt, \{Alexander U.\} and John Chen and Friedemann Paul and Joachim Havla and Ayse Altintas and Saif Huda and Anu Jacob and Jaqueline Palace",

note = "Publisher Copyright: {\textcopyright} 2022 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.",

year = "2022",

month = sep,

doi = "10.1002/ana.26440",

language = "English",

volume = "92",

pages = "476--485",

journal = "Annals of Neurology",

issn = "0364-5134",

publisher = "John Wiley \& Sons Inc.",

number = "3",

}

TY - JOUR

T1 - Longitudinal Retinal Changes in MOGAD

AU - with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group

AU - Oertel, Frederike Cosima

AU - Sotirchos, Elias S.

AU - Zimmermann, Hanna G.

AU - Motamedi, Seyedamirhosein

AU - Specovius, Svenja

AU - Asseyer, Eva Susanna

AU - Chien, Claudia

AU - Cook, Lawrence

AU - Vasileiou, Eleni

AU - Filippatou, Angeliki

AU - Calabresi, Peter A.

AU - Saidha, Shiv

AU - Pandit, Lekha

AU - D'Cunha, Anitha

AU - Outteryck, Olivier

AU - Zéphir, Hélène

AU - Pittock, Sean

AU - Flanagan, Eoin P.

AU - Bhatti, M. Tariq

AU - Rommer, Paulus S.

AU - Bsteh, Gabriel

AU - Zrzavy, Tobias

AU - Kuempfel, Tania

AU - Aktas, Orhan

AU - Ringelstein, Marius

AU - Albrecht, Philipp

AU - Ayzenberg, Ilya

AU - Pakeerathan, Thivya

AU - Knier, Benjamin

AU - Aly, Lilian

AU - Asgari, Nasrin

AU - Soelberg, Kerstin

AU - Marignier, Romain

AU - Tilikete, Caroline Froment

AU - Cobo Calvo, Alvaro

AU - Villoslada, Pablo

AU - Sanchez-Dalmau, Bernardo

AU - Martinez-Lapiscina, Elena H.

AU - Llufriu, Sara

AU - Green, Ari J.

AU - Yeaman, Michael R.

AU - Smith, Terry J.

AU - Brandt, Alexander U.

AU - Chen, John

AU - Paul, Friedemann

AU - Havla, Joachim

AU - Altintas, Ayse

AU - Huda, Saif

AU - Jacob, Anu

AU - Palace, Jaqueline

PY - 2022/9

Y1 - 2022/9

N2 - Objective: Patients with myelin oligodendrocyte glycoprotein antibody (MOG-IgG)-associated disease (MOGAD) suffer from severe optic neuritis (ON) leading to retinal neuro-axonal loss, which can be quantified by optical coherence tomography (OCT). We assessed whether ON-independent retinal atrophy can be detected in MOGAD. Methods: Eighty patients with MOGAD and 139 healthy controls (HCs) were included. OCT data was acquired with (1) Spectralis spectral domain OCT (MOGAD: N = 66 and HCs: N = 103) and (2) Cirrus high-definition OCT (MOGAD: N = 14 and HCs: N = 36). Macular combined ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) were quantified. Results: At baseline, GCIPL and pRNFL were lower in MOGAD eyes with a history of ON (MOGAD-ON) compared with MOGAD eyes without a history of ON (MOGAD-NON) and HCs (p < 0.001). MOGAD-NON eyes had lower GCIPL volume compared to HCs (p < 0.001) in the Spectralis, but not in the Cirrus cohort. Longitudinally (follow-up up to 3 years), MOGAD-ON with ON within the last 6–12 months before baseline exhibited greater pRNFL thinning than MOGAD-ON with an ON greater than 12 months ago (p < 0.001). The overall MOGAD cohort did not exhibit faster GCIPL thinning compared with the HC cohort. Interpretation: Our study suggests the absence of attack-independent retinal damage in patients with MOGAD. Yet, ongoing neuroaxonal damage or edema resolution seems to occur for up to 12 months after ON, which is longer than what has been reported with other ON forms. These findings support that the pathomechanisms underlying optic nerve involvement and the evolution of OCT retinal changes after ON is distinct in patients with MOGAD. ANN NEUROL 2022;92:476–485.

AB - Objective: Patients with myelin oligodendrocyte glycoprotein antibody (MOG-IgG)-associated disease (MOGAD) suffer from severe optic neuritis (ON) leading to retinal neuro-axonal loss, which can be quantified by optical coherence tomography (OCT). We assessed whether ON-independent retinal atrophy can be detected in MOGAD. Methods: Eighty patients with MOGAD and 139 healthy controls (HCs) were included. OCT data was acquired with (1) Spectralis spectral domain OCT (MOGAD: N = 66 and HCs: N = 103) and (2) Cirrus high-definition OCT (MOGAD: N = 14 and HCs: N = 36). Macular combined ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) were quantified. Results: At baseline, GCIPL and pRNFL were lower in MOGAD eyes with a history of ON (MOGAD-ON) compared with MOGAD eyes without a history of ON (MOGAD-NON) and HCs (p < 0.001). MOGAD-NON eyes had lower GCIPL volume compared to HCs (p < 0.001) in the Spectralis, but not in the Cirrus cohort. Longitudinally (follow-up up to 3 years), MOGAD-ON with ON within the last 6–12 months before baseline exhibited greater pRNFL thinning than MOGAD-ON with an ON greater than 12 months ago (p < 0.001). The overall MOGAD cohort did not exhibit faster GCIPL thinning compared with the HC cohort. Interpretation: Our study suggests the absence of attack-independent retinal damage in patients with MOGAD. Yet, ongoing neuroaxonal damage or edema resolution seems to occur for up to 12 months after ON, which is longer than what has been reported with other ON forms. These findings support that the pathomechanisms underlying optic nerve involvement and the evolution of OCT retinal changes after ON is distinct in patients with MOGAD. ANN NEUROL 2022;92:476–485.

UR - https://www.scopus.com/pages/publications/85134148770

U2 - 10.1002/ana.26440

DO - 10.1002/ana.26440

M3 - Article

C2 - 35703428

AN - SCOPUS:85134148770

SN - 0364-5134

VL - 92

SP - 476

EP - 485

JO - Annals of Neurology

JF - Annals of Neurology

IS - 3

ER -

Longitudinal Retinal Changes in MOGAD

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